Corpuscles of Stannius development requires FGF signaling

被引:7
作者
Klingbeil, Konstantin [1 ]
Nguyen, Thanh Quang [1 ]
Fahrner, Andreas [1 ]
Guthmann, Clara [1 ]
Wang, Hui [1 ]
Schoels, Maximilian [1 ]
Lilienkamp, Miriam [1 ]
Franz, Henriette [2 ]
Eckert, Priska [1 ]
Walz, Gerd [1 ,3 ,4 ]
Yakulov, Toma Antonov [1 ]
机构
[1] Albert Ludwigs Univ Freiburg, Fac Med, Fribourg, Switzerland
[2] Univ Basel, Dept Biomed, Basel, Switzerland
[3] Albert Ludwigs Univ Freiburg, Signaling Res Ctr BIOSS, Albertstr 19, D-79104 Freiburg, Germany
[4] Albert Ludwigs Univ Freiburg, Signaling Res Ctr CIBSS, D-79104 Freiburg, Germany
关键词
Kidney; Fibroblast growth factor (FGF); Zebrafish; Wnt signaling; Development; Corpuscles of Stannius; Pronephros; Cpe; RETINOIC ACID; ZEBRAFISH NEPHROGENESIS; RECEPTOR; SEGMENTATION; ACTIVATION; EXPRESSION; RESPONSES;
D O I
10.1016/j.ydbio.2021.10.005
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The corpuscles of Stannius (CS) represent a unique endocrine organ of teleostean fish that secrets stanniocalcin-1 (Stc1) to maintain calcium homeostasis. Appearing at 20-25 somite stage in the distal zebrafish pronephros, stc1expressing cells undergo apical constriction, and are subsequently extruded to form a distinct gland on top of the distal pronephric tubules at 50 h post fertilization (hpf). Several transcription factors (e.g. Hnf1b, Irx3b, Tbx2a/b) and signaling pathways (e.g. Notch) control CS development. We report now that Fgf signaling is required to commit tubular epithelial cells to differentiate into stc1-expressing CS cells. Inhibition of Fgf signaling by SU5402, dominant-negative Fgfr1, or depletion of fgf8a prevented CS formation and stc1 expression. Ablation experiments revealed that CS have the ability to partially regenerate via active cell migration involving extensive filopodia and lamellipodia formation. Activation of Wnt signaling curtailed stc1 expression, but had no effect on CS formation. Thus, our observations identify Fgf signaling as a crucial component of CS cell fate commitment.
引用
收藏
页码:160 / 171
页数:12
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